To the Editor:

As reported in CHEST (June 2002), several studies1–4
have suggested that selective cyclooxygenase-2 (COX-2) inhibitors, rofecoxib and celecoxib, are safe for use by patients with aspirin-induced asthma and who are intolerant to cyclooxygenase-1 (COX-1) inhibitors. However, there are less than 140 patients in all four of these studies. We wish to report a 78-year-old woman with asthma, well-controlled with beclomethasone and albuterol inhalers for at least 3 years, who developed an acute exacerbation of asthma symptoms after three doses of rofecoxib, each 25 mg. This patient had previously had an adverse reaction to aspirin and since then had avoided aspirin and all nonsteroidal antiinflammatory medications, using only acetaminophen for pain relief. The rofecoxib was stopped, and she responded to nebulized albuterol and prednisone therapy, and her symptoms improved.

Up to 10% patients with moderate-to-severe asthma are sensitive to aspirin. These patients may have life-threatening asthma if they take aspirin or nonselective cyclooxygenase inhibitors. The studies cited1–4
suggest that inhibition of COX-1 is the essential initiator of adverse outcomes in patients with aspirin-sensitive asthma. Therefore, highly selective COX-2 inhibitors should not affect these patients.

In our patient, one possibility is that she was unusually sensitive to the minimal COX-1 inhibition in rofecoxib. In any case, we recommend caution when prescribing selective COX-2 inhibitors to patients with aspirin-sensitive asthma.

To the Editor:

We appreciate the comments of Drs. Passero and Chowdhry regarding our study of selective cyclooxygenase-2 (COX-2) inhibitors in patients with aspirin-induced asthma (AIA), which was published in CHEST (June 2002).1
We agree that recent reports about the safety of such inhibitors in patients with AIA were carried out with a limited number of patients1–4
; as we suggested in our article, further challenge procedure studies performed with higher doses of rofecoxib and other highly selective COX-2 inhibitors on larger series of patients with AIA are necessary in order to achieve the safety of such new drugs in patients with AIA.

The authors mentioned that the acute exacerbation of asthma developed after three doses of rofecoxib, each 25 mg. We supposed each rofecoxib dose was taken once per day on 3 consecutive days, and not all three doses in 1 single day. There are no published data at present about the safety of COX-2 inhibitors in patients with AIA receiving high doses, and we regard that studies concerning this point are necessary.

It is known that the degree of sufficient enzymatic inhibition to induce bronchial narrowing in patients with AIA is an individual hallmark5
; therefore, we believe that oral challenges with progressive doses of the drug (rofecoxib or celecoxib) would have been done until a therapeutic and tolerable dose was reached. Nevertheless, despite the safety demonstrated by the new highly selective COX-2 inhibitors, caution when prescribing any type of nonsteroidal anti-inflammatory drugs in patients with AIA should always be recommended.

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